This study seeks to evaluate, by the use of an infant primate model, the increasingly supported hypothesis that the Sudden Infant Death Syndrome (S.I.D.S.), does not necessarily involve a precipitous series of terminal events without antecedent pathology, but that victims of this disorder might be characterized by predisposing physiologic states, particularly chronic hypoxemia resulting from deficient ventilatory performance. Chronic hypoxia states will be induced in infant monkeys by three methods. I. Sustained exposure to low oxygen in a closed system incubator. II. Production of diffuse ischemic lesions of the brainstem to interfere with ventilatory regulation, and III. Antenatal exposure to hypoxemia by hypotensive reduction of placental circulation and caesarean delivery into an oxygen deficient environment. Using respiratory function measures and blood gas analysis the infants will be compared with a control population with respect to adequacy of respiratory control factors including basal respiratory function, response to changes in respiratory gas composition and characteristics of laryngeal reflexes. Tissues of the animals will be prepared for microscopy and examined quantitatively for indices of chronic hypoxemia, including proliferation of brainstem astroglia, lung artery changes, right ventricular hypertrophy, hepatic hematopoietic tissue retention, bone marrow hematopoiesis, brown fat retention and increased adrenal chromaffin tissue.